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Studies on the physiological defect in rII mutants of bacteriophage T4


, : Studies on the physiological defect in rII mutants of bacteriophage T4. Journal of Molecular Biology 16(2): 503-522

The inability of rII mutants of bacteriophage T4 to multiply in strains of Escherichia coli lysogenic for \ is shown to be due to an inhibition by monovalent cations usually present in culture media. If monovalent cations are omitted from the medium, rII mutants and the wild-type phage multiply normally, provided sufficient osmotic pressure is maintained by, for example, salts of divalent cations or sucrose. One effect of inhibitory concentration of monovalent cations is to avert the uptake of magnesium by rII-infected cells early in the latent period. Evidence is presented that a deficit in phosphorylation might be the primary cause of cessation of phage development in rII-infected E. coli KB: (1) Incorporation of 32P into ATP (as well as into other phosphate-containing compounds). drops after rII infection, while the uptake of inorganic phosphate by cells continues normally. (2) Simultaneous labeling by 32P and [14C] uridine showed that the failure in phosphorylation of nucleotides precedes the failure in the synthesis of nucleid acid. (3) The ATP level of bacteria drops after infection with rII. (4) The drop in phosphorylation activity in rll-infected cells appears immediately after infection, whereas other metabolic activities continue normally for about 10 minutes. Various enzymes concerned in ATP metabolism were examined, but all showed about the same activity levels in r+- and rll-infected cells. An extensive leakage of NAD from rll-infected cells was observed, but the relation between loss of NAD and the failure in phosphorylation is not clear.

US$19.90

PMID: 5954174

DOI: 10.1016/S0022-2836(66)80188-2


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